Fig. 1: BET inhibition represses adaptive RTK expression following BRAF/MEK inhibitors treatment in BRAF-mutant melanoma. | British Journal of Cancer

Fig. 1: BET inhibition represses adaptive RTK expression following BRAF/MEK inhibitors treatment in BRAF-mutant melanoma.

From: Targeting BRD/BET proteins inhibits adaptive kinome upregulation and enhances the effects of BRAF/MEK inhibitors in melanoma

Fig. 1: BET inhibition represses adaptive RTK expression following BRAF/MEK inhibitors treatment in BRAF-mutant melanoma.The alternative text for this image may have been generated using AI.

a RPPA analysis for the BRAF-mutant human melanoma cell lines, A375, 1205Lu, and M238, after 24 h of treatment with BRAFi/MEKi (dabrafenib, 50 nM + trametinib, 5 nM). RPPA scores for proteins involved in RTK signalling that were statistically significant (p < 0.05) with BRAFi/MEKi versus vehicle (DMSO) treatment samples. b Western blots for RPPA-identified proteins in a after treatment with BRAFi/MEKi over a 24-h time course. c RPPA analysis for the cell lines, A375, 1205Lu, and M238, after 24 h of treatment with BRAFi/MEKi (dabrafenib, 50 nM + trametinib, 5 nM) Âħ BETi in a dose-dependent manner (either JQ1: 0.01, 0.1, 1, and 5 ÎĵM or PLX51107: 1, 2, and 4 ÎĵM). Shown are antibodies for proteins involved in RTK signalling found to be statistically significant (p < 0.05) in at least one comparison between BRAFi/MEKi Âħ BETi-treated groups. d Representative Western blots of three (n = 3) independent experiments for RTK proteins after 24 h of combination treatment with BRAFi/MEKi Âħ BETi in a dose-dependent manner for the doses described above.

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